ebook img

Skeletal Aging and Osteoporosis: Biomechanics and Mechanobiology PDF

260 Pages·2013·5.246 MB·English
Save to my drive
Quick download
Download
Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.

Preview Skeletal Aging and Osteoporosis: Biomechanics and Mechanobiology

Studies in Mechanobiology, Tissue Engineering and Biomaterials Volume 5 Series Editor Amit Gefen, Ramat Aviv, Israel For furthervolumes: http://www.springer.com/series/8415 Matthew J. Silva Editor Skeletal Aging and Osteoporosis Biomechanics and Mechanobiology 123 Editor Matthew J.Silva Department of OrthopaedicSurgery Washington University, St.Louis MO, USA ISSN 1868-2006 ISSN 1868-2014 (electronic) ISBN 978-3-642-18052-1 ISBN 978-3-642-18053-8 (eBook) DOI 10.1007/978-3-642-18053-8 SpringerHeidelbergNewYorkDordrechtLondon LibraryofCongressControlNumber:2012943364 (cid:2)Springer-VerlagBerlinHeidelberg2013 Thisworkissubjecttocopyright.AllrightsarereservedbythePublisher,whetherthewholeorpartof the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation,broadcasting,reproductiononmicrofilmsorinanyotherphysicalway,andtransmissionor informationstorageandretrieval,electronicadaptation,computersoftware,orbysimilarordissimilar methodology now known or hereafter developed. Exempted from this legal reservation are brief excerpts in connection with reviews or scholarly analysis or material supplied specifically for the purposeofbeingenteredandexecutedonacomputersystem,forexclusiveusebythepurchaserofthe work. Duplication of this publication or parts thereof is permitted only under the provisions of theCopyrightLawofthePublisher’slocation,initscurrentversion,andpermissionforusemustalways beobtainedfromSpringer.PermissionsforusemaybeobtainedthroughRightsLinkattheCopyright ClearanceCenter.ViolationsareliabletoprosecutionundertherespectiveCopyrightLaw. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publicationdoesnotimply,evenintheabsenceofaspecificstatement,thatsuchnamesareexempt fromtherelevantprotectivelawsandregulationsandthereforefreeforgeneraluse. While the advice and information in this book are believed to be true and accurate at the date of publication,neithertheauthorsnortheeditorsnorthepublishercanacceptanylegalresponsibilityfor anyerrorsoromissionsthatmaybemade.Thepublishermakesnowarranty,expressorimplied,with respecttothematerialcontainedherein. Printedonacid-freepaper SpringerispartofSpringerScience+BusinessMedia(www.springer.com) Preface Whyanotherbonebook?Iagreedtoeditthisbookbecausethereisnosimilarbook thatIknow.Thereareexcellenttextscoveringbonemechanics(e.g.,byCowin)and musculoskeletalbiomechanics(e.g.,byBartel,DavyandKeaveny;Martin,Burrand Sharkey; Mow and Huiskes), and equally excellent (and massive) texts covering bone biology/aging/osteoporosis (e.g., by Marcus, Feldman, Nelson and Rosen; Rosen,GlowackiandBilezikian).Inthesetexts,thetopicofbonebiomechanicsand agingisjustasmallpartofalargeragenda.Heremygoalwastonarrowthefocus anddevoteanentirevolumetothequestions:Whatchangesinbone(s)occurwith aging or osteoporosis that are relevant to bone strength? How do we predict bone strength?Howdoosteoporosisdrugsaffectbonestrength?Whatchangesoccurwith agingthatarerelevanttobonemechanobiology?Therehasbeenalotofresearchon thesequestionsinthepast40years,butnosinglevolumethatattemptstoreviewit. The assembled chapters offer such a review. They highlight many age-related phenomenathatareirrefutable,butalsopointtoissuesthataredebatableornotfully explored. Aging studies are difficult whether they use animals, human subjects or postmortemmaterial,andthereisstillmuchworktobedone. The first five chapters address the biomechanics question. Chapter 1 covers changes in bone structure and strength at the whole-bone level, while Chaps. 2–5 cover changes in properties at the trabecular and cortical bone tissue level, with focusonmicrostructure,compositionandmicrodamage.Chapter6reviewsrecent attemptsatintegratingourknowledgeofstructure,strengthandloadingtopredict fracturerisk.Chapter7reviewstheeffectsofosteoporosisdrugtreatmentsonbone strength and fracture. The next four chapters address the mechanobiology question. Chapter 8 reviews mechanoresponsiveness and aging at the cellular level. Chapters 9 and 10 review mechanoresponsiveness in animal experiment, with focus on aging and sex hormones, respectively. Lastly, Chap. 11 reviews clinicalevidencethatloadinginfluencesboneinthesettingofaging/osteoporosis. Even a modest volume like this takes a large collective effort. I heartily thank eachoftheauthorswhocontributedchapterstothisvolume.Theygenerouslygave of their time to write and revise their chapters. I hope that readers will find our efforts were worthwhile. v Contents Age-Related Changes in Whole-Bone Structure and Strength . . . . . . . 1 Matthew J. Silva and Karl J. Jepsen Characterisation of Trabecular Bone Structure . . . . . . . . . . . . . . . . . 31 Ian H. Parkinson and Nicola L. Fazzalari Cortical Bone Mechanics and Composition: Effects of Age and Gender. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Xiaodu Wang Bone Microdamage and Its Contributions to Fracture . . . . . . . . . . . . 87 Lamya Karim and Deepak Vashishth Changes in Cortical Bone Mineral and Microstructure with Aging and Osteoporosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105 Janardhan Yerramshetty and Ozan Akkus Factor of Risk for Fracture. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133 Dennis E. Anderson and Mary L. Bouxsein Bisphosphonates and PTH for Preventing Fractures. . . . . . . . . . . . . . 151 David B. Burr and Matthew R. Allen Bone Cell Mechanoresponsiveness . . . . . . . . . . . . . . . . . . . . . . . . . . . 177 Damian C. Genetos and Christopher R. Jacobs vii viii Contents The Effect of Aging on Skeletal Mechanoresponsiveness: Animal Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 Akhilesh A. Kotiya and Matthew J. Silva Skeletal Mechanoresponsiveness: Effects of Sex Hormones . . . . . . . . . 217 Katherine M. Melville, Natalie H. Kelly and Marjolein C. H. van der Meulen Effects of Exercise and Physical Interventions on Bone: Clinical Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 Wendy M. Kohrt, Karen L. Villalon and Daniel W. Barry Author Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 Age-Related Changes in Whole-Bone Structure and Strength Matthew J. Silva and Karl J. Jepsen Abstract We review data on age-related changes in bone geometry of relevance to whole-bone strength, as well as the limited data on changes in strength. Con- sistentlyacrossmanysites,womenhavebonesthataresmaller(by15–30 %)than age-matchedmen,andthusareweaker.Inbothwomenandmen,modestperiosteal expansion of the diaphysis occurs throughout life, but this is accompanied by a faster rate of medullary expansion, especially inwomen. The net result is an age- relateddecreaseincorticalboneatmostsitesinwomen,butnegligiblechangesin men. At metaphyseal sites there is also modest periosteal expansion as well as endosteal expansion and net cortical bone loss. But the dominant change with agingisdecreasedtrabecularbonedensity,withmoststudiesshowinggreaterrates of decline in women than men. These effects are especially pronounced at the proximal femur and vertebra.Changes inwhole-bonestrength with aging are less well documented. Available data (from mechanical tests and computer models) suggest modest declines in diaphyseal strength in women but not men, and much greater declines in strength of the proximal femur and vertebra. Women and men appeartoloseproximalfemurstrengthatsimilarrates,althoughthedeclinestarts earlier in women. Also, both women and men lose vertebral strength with aging, with some data indicating a faster decline in women but other indicating M.J.Silva(&) DepartmentofOrthopaedicSurgery,WashingtonUniversitySchoolofMedicine, SaintLouis,Missouri63110,USA e-mail:[email protected] K.J.Jepsen DepartmentofOrthopaedicSurgery,UniversityofMichiganAnnArbor, Michigan48109,USA e-mail:[email protected] StudMechanobiolTissueEngBiomater(2013)5:1–30 1 DOI:10.1007/8415_2012_137 (cid:2)Springer-VerlagBerlinHeidelberg2012 PublishedOnline:13June2012 2 M.J.SilvaandK.J.Jepsen equivalentratesofdecline.Inconclusion,thereareimportantage-relatedchanges in bone structure and density that affect whole-bone strength. Additional studies measuring whole-bone strength with aging are needed. 1 Introduction Bonesarestructuralentitiesthatareincreasinglysusceptibletofracturewithaging. Age-related/osteoporoticfracturesoccuratanestimatedrateof2millionperyearin the U.S. with corresponding high costs in economic terms, quality of life, and increasedmortality[1].Thecausesoftheincreaseinfractureincidencewithageare multifactorial, but can generally be grouped into factors affecting applied loading (e.g.,bodyweight,impactfromfallsorothertrauma)andfactorsaffectingstructural (whole-bone)strength.Becausethemechanicalbehaviorofastructuredependson its geometric and its material properties, changes in geometry and material prop- ertiesofboneswithageinfluencewhole-bonestrength.Thechangesthatoccurinthe materialpropertiesofbonewithageincludedensity,microstructure,composition, etc., and are considered in other chapters in this volume (‘‘Characterisation of TrabecularBoneStructure,CorticalBoneMechanicsandComposition:Effectsof AgeandGender,BoneMicrodamageanditsContributionstoFracture,Changesin Cortical Bone Mineral and Microstructure with Aging and Osteoporosis’’, ‘‘Bone MicrodamageanditsContributionstoFracture’’,ChangesinCorticalBoneMineral and Microstructure with Aging and Osteoporosis’’). Of primary interest in this chapter are the changes in bone structure (i.e., size and shape, also called mor- phology) that are documented to occur with aging. We also consider the limited availabledataonwhole-bonemechanicalpropertiesandaging. There are many descriptors of bone morphology, but based on engineering mechanicswefocusontwogeometricpropertiesofparticularrelevancetowhole- bone strength: cross-sectional area and moment of inertia. For example, for a cylindrical structure like the diaphysis (shaft) of a long bone (Fig. 1), the theo- retical strength under axial and bending loading are given by: F ¼ r x A fail fail M ¼ r x I = c fail fail where F is the axial failure force (structural strength as it pertains to failure fail under purely compressive or tensile loads), M is the bending failure moment fail (structuralstrengthasitpertainstofailureunderbendingloads),r isthefailure fail stress (material strength), A is the cross-sectional area, I is the cross-sectional moment of inertia (also called the second moment of area), and c is the distance from the center of the cross-section to the outer most point on the surface. For a solidcylinderwithacircularcross-section:A = pD2/4,I = pD4/64,andc = D/2, where D is the diameter. (See Fig. 1 for additional equations.) From these two Age-RelatedChanges 3 Fig.1 Sketch of idealized a diaphyseal and b metaphyseal cross-sections of bones. For the hollow circular cross-section of a: total area, TA=pD2/4; medullary area, MA=pD2/4; P M corticalbonearea,CA=TA-MA=p(D2-D2)/4;bonemomentofinertia=p(D4-D4)/64 P M P M equations we note that structural strength depends directly on r (material) and fail eitherAorI(geometry),whichinturndependondiametersquaredorraisedtothe power four. Area is essentially a measure of the amount of bone in the cross- section, while moment of inertia is a measure reflecting both the amount of bone and how it is distributed. These simple relationships motivate our interest in area and moment of inertia as two key measures of bone size. Also of interest are diameter and section modulus, defined as I/c. Bones are dynamic structures that change throughout life. In this chapter, we review the published data on changes in bone structure with aging. We consider changesin the diaphyseal regionsof long bones (e.g., femur, tibia, radius), which are comprised mostly ofcorticalbone,andchangesat the ends of long bones and in short bones (e.g., vertebra), which are comprised of a mix of cortical and trabecular bone. These latter sites are of particular clinical relevance as the most commonfracturesitesarethevertebra,distalradiusandproximalfemur.Wefocus primarily on bone geometry, but also consider whole-bone mechanical properties where data are available. We also discuss recent work showing that material and geometric properties, often considered to be independent contributors to whole- bone strength, are probably not independent. 2 Diaphyseal Changes with Age 2.1 Cross-Sectional Geometry Even after rapid skeletal growth ends in the third decade of life, the diaphyses of long bones continue to change via periosteal and endocortical expansion. The net changes in geometry indicate that bone apposition prevails at the periosteum, 4 M.J.SilvaandK.J.Jepsen while resorption prevails at the endocortex. Generally, these changes occur throughout life, although the rates ofexpansion are site- and sex-dependent. Here wereviewchangeswithageinthediaphysealcross-sectionsofbones,specifically subperiosteal area (also called total area, TA), medullary area (MA) and cortical bone area (CA). 2.1.1 Lower Extremity: Femur and Tibia Thesizeofthefemoralandtibialdiaphysisinwomenisapprox.20 %smallerthan age-matchedmen.Thisfigureisanaverageacrossthestudieswereviewed[2–9], and refers to both total area and cortical area. The phenomenon of diaphyseal expansion of weight-bearing long bones with aging has been recognized for at least 50 years. Early studies were based on femoral radiographs [10] or physical sections from cadaver bones [2, 4, 5]. In a well-known ‘‘classic’’ study, Ruff and Hayes [5] reported that women do not exhibitage-relatedperiostealexpansionasmendo,althoughthisresultwasbased on only 37 female donors, and later studies have contradicted this conclusion. More recently, non-invasive imaging methods such as peripheral quantitative computed tomography (pQCT) have been used to determine true cross-sectional geometry in large numbers of subjects [3, 6–9]. The findings of several classic and recent studies are summarized in Table 1, whereage-relatedchangesarepresentedasaveragepercentchangeper10yearsof lifebasedonlinearregressionanalysis. Theseresultssupportaconsistentpattern. In women, the periosteum expands at a slow rate from young adulthood (3rd decade) to old age, resulting in an average increase in total area of *2 % per decade. However, the endocortex expands at a faster rate, resulting in an average increaseinmedullaryarea(MA)of*13 %/decadeandanetlossofcorticalbone area of *3 %/decade. In men, the rate of periosteal expansion is similar as in women (*2 %/decade), but the medullary expansion is notably slower (*7 %/ decade) and the net change in cortical area is negligible (-1 %/decade). Because momentofinertiaisrelatedtothefourthpowerofbonediameter,theage-changes inmomentofinertiareflectprimarilytheage-changesintotalareaandtoalesser butimportantextent theage-changesincortical area.Bothparameters areneeded tofullyunderstandtheimpact ofperiostealexpansionandendocorticalresorption ontheresistancetobendingandtorsionalloading.Dataonage-changesinmoment of inertia (or section modulus) are limited. The majority of reports indicate no significant age-effect on moment of inertia, due in part to statistically under- poweredstudies(i.e.,typeIIerror).Ofthestudiesusing3Dimagingmethodswith largesamplesizes,Russoetal.[6]reportedadeclineindensity-weightedmoment of inertia in women but no change in men, while Yuen et al. [9] reported a slight decline (-2 %/decade) in both women and men. A decline with aging might be interpreted as a failure of biological processes to maintain mechanical function throughout life.

See more

The list of books you might like

Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.